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1
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Dopalacze - jak to działa?

100%
Golembiowska K.
Wszechświat
|
2013
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tom 114
|
nr 01-03
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Co dopalacze mogą zrobić z naszym mózgiem

100%
Golembiowska K.
Wszechświat
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2011
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tom 112
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nr 01-03
3

Effect of VMAT2 inhibition on glutamate and adenosine in rat frontal cortex

63%
Kaminska K., Golembiowska K.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Our earlier studies showed that inhibition of VMAT2 caused depletion of dopamine in rat striatum accompanied with outflow of glutamate and production of hydroxyl radical. Inhibition of VMAT2 is observed in an early phase of Parkinson’s Disease (PD) as evidenced by PET studies in PD patients and in non-human primates. Recently it is observed that many neurons also release a classical transmitter other than the one with which they are usually associated. It is shown that neurons releasing monoamines can also release the excitatory transmitter glutamate. All neurons contain glutamate for its role in protein synthesis and metabolism, but they also express VGLUTs required for excitotoxic glutamate release. Moreover, it is also shown that several catecholamine cells such as VTA dopamine neurons are able corelease glutamate. Disturbed function of both, VMAT 2 and VGLUT may start catecholamine neurons degeneration that occurs at the early pre-clinical stage of PD. Accumulation of cytosolic dopamine may be neurotoxic for neurons through the generation of free radicals. Similarly, glutamate released from neurons or glial cells via GLT-1 transporter or cystine-glutamate exchanger or purinergic P2X7 receptor may stimulate glutamate receptors on various cells, induce increase in intracellular calcium which leads to excitotoxicity and generation of free radicals. ATP is required for packing of dopamine or glutamate in neuronal and glial vesicles and disturbed vesicular function results in ATP metabolism to adenosine in the presence of 5’-nucleotidase. In our study we tried to understand the early changes in dopamine synapses and glial cell responses which may provide insights on PD pathology. We injected animals with reserpine to inhibit vesicular transport and measured veratridine-evoked (100 µM) dopamine, glutamate and adenosine release using microdialysis in frontal cortex of freely moving rats. Extracellular dopamine, adenosine and glutamate were assayed by HPLC with electrochemical, fluorescenece and VIS detection. Reserpine at a single dose of 2.5 mg/kg increased veratridine-evoked glutamate release to 200% and adenosine release to 5 000% of baseline 20 h after administration. Reserpine at a dose of 0.25 mg/kg given repeatedly for 14 days increased evoked-glutamate release to maximum 210% and adenosine to 1 400% of baseline. At the same time veratridine-induced DA release was also markedly increased as compared to control animals. Veratridine-evoked glutamate and adenosine release were increased by 150 and 600% of baseline, respectively in intact rats. Obtained results indicate that under conditions of damaged vesicular transport there is significant overflow of glutamate and adenosine as well as increase in dopamine release in the rat frontal cortex. Marked increase in extracellular adenosine release may lead to activation of adenosine A2A receptors located in glutamate terminals or glial cells causing damage through induction of oxidative stress by glutamate or dopamine. Corelease of neurotransmitters and neuromodulators from neuronal or glial cells with disturbed vesicular transport may underline cortical pathology observed in PD.
4

Involvement of adenosine receptors in L-DOPA-induced oxidative stress in rat striatum

63%
Dziubina A., Golembiowska K.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
|
nr 4
5

The effect of p-chloroamphetamine and p-chlorophenylalanine on the level of thyrotropin releasing hormone (TRH) and its receptors in the central nervous system of the rat

51%
Przegalinski E., Jaworska L., Golembiowska K.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 3
6

L--DOPA-induced free radicals generation in rat striatum

51%
Golembiowska K., Kowalska M., Dziubina A.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
|
nr 3
7

MPEP protects against methamphetamine toxicity in rats

51%
Konieczny J., Golembiowska K., Ossowska K., Wolfarth S.
Acta Neurobiologiae Experimentalis
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2001
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tom 61
|
nr 3
8

A2A adenosine receptor antagonists effet on hydroxyl radical generation in DA depleted striatum with reserpine

51%
Golembiowska K., Dziubina A., Morelli M.
Acta Neurobiologiae Experimentalis
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2009
|
tom 69
|
nr 3
Although the cause of DA neurons neurodegeneration is still unknown, oxidative stress is paramount in the pathogenesis of Parkinson’s disease. An accumulation of cytosolic DA has been shown to be neurotoxic through the generation of free radicals (FR). Searching for FR scavengers, we studied the effect of selective A2A adenosine receptor antagonists, shown to have neuroprotective properties, on hydroxyl radical (HR) production in rat striatum with reserpine impaired DA storage. We found an increase in extracellular glutamate and HR levels in DA-depleted striatum. CSC (1 mg/kg), ZM 241385 (3 mg/ kg) and L-DOPA (25 mg/kg) normalized glutamate release and combination of A2A antagonists and L-DOPA showed similar effect. CSC increased DA and HR levels but ZM 241385 given alone did not affect DA nor HR levels. L-DOPA enhanced DA extracellular level but did not change the production of HR. Combination of L-DOPA and CSC further elevated DA extracellular level and markedly increased HR production while combination of L-DOPA and ZM 241385 attenuated, enhanced by L-DOPA DA level and had no effect on HR production. This data suggests that disrupted balance between DA and glutamate in DA depleted nigrostriatal neurons results in generation of neurotoxic HR. Both A2A antagonists, like L-DOPA, redress the DA/glutamate balance. However, A2A antagonists in combination with L-DOPA show different pharmacological profi le in their effect on DA release and subsequent generation of HR.
9

GABAergic transmission in the rat dorsal raphe nucleus is moduated by the 5-HT 7 receptor

39%
Sowa J., Kusek M., Kaminska M., Golembiowska K., Tokarski K., Hess G.
Acta Neurobiologiae Experimentalis
|
2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: The 5-HT7 receptor is one of the several 5-HT receptor subtypes which are expressed in DRN neurons. Some previous findings suggested that 5-HT7 receptors in the DRN are localized on local GABAergic interneurons, which modulate the activity of 5-HT projection neurons. The aims of this study were to determine how the 5-HT7 receptor activation and blockade influence the GABAergic synaptic input to presumed 5-HT DRN neurons and whether blockade of the 5-HT7 receptor would affect the release and metabolism of 5-HT in the prefrontal cortex in vivo. METHODS: Male Wistar rats, with microdialysis probes implanted in the PFC, received ip injections of 5-HT7 receptor antagonist, SB 269970. 5-HT and 5-HIAA, were analyzed by HPLC. In another set of experiments whole-cell recordings were carried out from DRN slices. SB 269970 was used to block the 5-HT7 receptor. To activate the 5-HT7 receptor 5-CT was applied in the presence of WAY 100635. RESULTS: Ip administration of SB269970 induced an increase in the level of 5-HT and 5-HIAA in PFC. SB 269970 application resulted in a depolarization of presumed DRN projection neurons and in an increase in the spontaneous firing frequency. A hyperpolarization of the cells and a decrease in the spontaneous firing frequency were observed after activation of the 5-HT7 receptor. Blockade of the 5-HT7 receptor caused a decrease in the mean frequency of sIPSCs, while its activation induced an increase. CONCLUSIONS: These results show that blockade of the 5-HT7 receptor enhances the release and metabolism of 5-HT in the PFC. This effect appears to be mediated by depolarization and enhanced firing of DRN serotonergic neurons resulting from a decreased inhibitory synaptic input received by the projection cells. Activation of the 5-HT7 receptor caused opposite effects on activity and the inhibitory input to putative DRN projection neurons. Support: National Science Centre Poland grant DEC-2013/11/B/ NZ4/04743.
10
Content available remote

Effect of venlafaxine and nicotine on the level of neurotransmitters and their metabolites in rat brains

39%
Czubak A., Nowakowska E., Golembiowska K., Kus K., Burda K., Metelska J.
Journal of Physiology and Pharmacology
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2010
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tom 61
|
nr 3
339-346
Nicotine (NIC) and venlafaxine (VEN) have been proved to exert antidepressant activity in both human and animals. The effect of antidepressant doses of NIC and VEN (our previous results) on noradrenergic (NA), dopaminergic (DA), serotoninergic (5-HT) neurotransmitters and their metabolites: DOPAC, HVA and 5-HIAA in rats’ hippocampus in freely moving rats were determined by microdialysis technique and HPLC method. Both drugs release 5-HT and NA, but VEN to a greater degree. DA level was affected only by VEN, however NIC extended the response of the DA system on VEN’s effect. Combined administration of drugs caused the greatest changes in the 5-HT system. Both drugs contributed to reduction in neurotransmitter biotransformation.
11

Chronic intraventricular infusion of MPP+ with alzet osmotic minipumps in rats as a model of parkinson's disease

39%
Kuter K., Kolasiewicz W., Zapala M., Kowalska M., Golembiowska K., Morelli M., Wardas J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
An underlying mechanism of degeneration in Parkinson’s disease (PD) is unknown. The animal models of PD, developed so far have certain disadvantages; hence a search for a new model of PD seems necessary. Chronic, unilateral, intraventricular delivery of MPP+ (0.284 and 0.428 mg/kg/day for 28 days) using an ALZET osmotic minipump, implanted s.c., produced a marked, dose-dependent loss of DA and its metabolites DOPAC and HVA (50–90%) in the striatum, ipsilateral to the infusion site. DA concentration was normal in the non-infused, right striatum. Also no changes in the 5-HT level were observed. The stereological counting of the number of dopaminergic neurons in the substantia nigra pars compacta (SNc), stained with the antibody against tyrosine hydroxylase, showed their 30–50% loss on the lesioned side. Those changes were accompanied with a diminished expression of mRNA for the dopamine transporter in the SNc (by ca. 30%). Additionally, in situ hybridization studies indicated an enhanced expression of mRNA for both adenosine A2A and dopamine D2 receptors in the striatum and diminished expression of mRNA for BDNF in the hippocampus. The obtained results showed that this chronic model of continuous, intracerebral infusion of MPP+ , produced a selective nigrostriatal DA cell loss and number of other neurochemical changes resembling PD. Study supported by the grant No. NN401 1137 33 (MS&HE) and by a statutory fund from the Institute of Pharmacology, PAS, Poland.
12
Content available remote

Intraperitoneal zinc administration increases extracellular zinc in the rat prefrontal cortex

39%
Opoka W., Sowa-Kucma M., Kowalska M., Bas B., Golembiowska K., Nowak G.
Journal of Physiology and Pharmacology
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2008
|
tom 59
|
nr 3
477-487
Single administration of zinc evokes pharmacological behavioral effects in rodents, while no brain zinc alterations were detected. The aim of the present study was to examine the effect of a single zinc hydroaspartate intraperitoneal (ip) administration on the extracellular (synaptic) zinc concentration in the rat prefrontal cortex. We used anodic stripping voltammetric (ASV) method of zinc determination in microdialysate, which assays the extracellular zinc concentration. We report that acute (65 mg/kg) zinc hydroaspartate administration (ip) increases the extracellular zinc by 48% in the rat prefrontal cortex. These data for the first time demonstrate: 1) utility of ASV zinc detection in brain microdialysates and 2) that single ip zinc administration increases brain (cortical) extracellular zinc pool. The results indicate zinc-induced fast brain penetration and may explain its rapid pharmacological effects.
13

Changes in glutamatergic transmission in the fronto-parietal cortex after chronic treatment with neuroleptics in rats

39%
Pietraszek M., Bijak M., Golembiowska K., Wardas J., Wolfarth S., Ossowska K.
Acta Neurobiologiae Experimentalis
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2001
|
tom 61
|
nr 3
14

Generation of transgenic mice with selective ablation of NMDA receptors in noradrenergic neurons

33%
Rodriguez Parkitna J., Tokarski K., Golembiowska K., Kubik J., Solecki W., Novak M., Schutz D., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2009
|
tom 69
|
nr 3
The brain’s noradrenergic system system provides essential modulation to neuronal activity, with well established roles in control of arousal and selective attention, as well as memory, learning and response to stress. We have generated a transgenic mouse, NR1DbhCre, with ablation of the essential NMDA receptor subunit NR1 (Grin1) in noradrenergic cells. Since no functional NMDA receptors may be formed in the absence of NR1, and their expression is restricted to the central nervous system, the NR1DbhCre mice have impaired glutamate-dependent plasticity in the central noradrenergic neurons, without observable alterations in the sympathetic system or the hypothalamus-pituitary-adrenal axis. Transgenic animals were born at expected ratios and developed normally, displaying no obvious impairments. The general anatomy of the noradrenergic system in the mutant mice was normal, no loss of cells was observed and noradrenaline content in the prefrontal cortex was not altered. Interestingly, preliminary electrophysiological analysis indicates that loss of functional NMDA receptors attenuates the spontaneous activity in current-clamped locus coeruleus noradrenergic neurons manually held at −50 mV potential. In summary the NR1DbhCre transgenic mice are a novel model for the study of the roles of the noradrenergic system in the central nervous system.
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